About

Nichole Broderick is an Assistant Professor in the Department of Biology at Johns Hopkins University. She joined Johns Hopkins in July 2020, after serving as an Assistant Professor in the Department of Molecular and Cell Biology and the Institute for Systems Genomics at the University of Connecticut. Prior to that, from 2013 to 2015, she was an Associate Research Scientist in the Molecular, Cellular & Developmental Biology Department at Yale University. Nichole earned her PhD from the University of Wisconsin-Madison, where she worked with Ken Raffa in Entomology and Jo Handelsman in Microbiology. She completed her postdoctoral research in the lab of Bruno Lemaitre at the École Polytechnique Fédérale de Lausanne (EPFL) in Lausanne, Switzerland. Her research focuses on the characterization of the gut microbiota of insect hosts and investigates how these microbial communities impact host physiology and susceptibility to disease. This work aims to understand the complex interactions between insect hosts and their gut microbes, shedding light on the role of microbiota in health and disease susceptibility in insect models.

Research topics

• Biology
• Genetics
• Computer Science
• Political Science
• Social Science
• Sociology
• Cell biology
• Data science
• Engineering
• Biotechnology
• Engineering ethics
• Computational biology
• Microbiology

Selected publications

• Microbiome contribution to <i>Indy</i> longevity in <i>Drosophila</i>

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-26

  articleOpen accessSenior authorCorresponding

  Abstract Reduction in the Indy (I’m not dead yet) gene, a plasma membrane citrate transporter, in Drosophila and its homolog in worms extends lifespan by promoting metabolic homeostasis. Indy reduction delays the onset of aging-associated pathology in the fly midgut, including preservation of intestinal barrier integrity and intestinal stem cell homeostasis. Gut microbiota has broad impacts on host metabolism, health, and aging. Age-related dysbiosis impairs intestinal barrier function and drives mortality. However, the underlying mechanisms that link increased microbial load to frailty and negative effects on health remain mostly unclear. Here we show that Indy heterozygote flies have significantly lower bacterial load and increased diversity during aging compared to controls. However, the presence of the microbiome was not required for Indy lifespan extension, though removal of microbes did enhance the effects of Indy reduction on longevity, suggesting potential interactions between the microbiome and Indy . Indy down-regulation was linked to reduced expression of the JAK/STAT signaling ligands Upd3 and Upd2 in the midgut of young flies, which likely contributes to preserved intestinal stem cell homeostasis. Altogether, our results suggest that Indy reduction impacts microbiome load and composition, which preserves gut homeostasis and extends lifespan through impacts on JAK/STAT signaling pathway. Significance Statement Indy is a fly homologue of mammalian SLC13A5 (mSLC13A5) plasma membrane citrate transporter, a central metabolic regulator involved in health, longevity, and disease. Reduction of fly Indy gene activity preserves metabolic and intestinal stem cell homeostasis and extends longevity. Gut microbiota impacts host metabolism, health, and aging. Here we show that Indy reduction prevents age-associated increases in bacterial load and expression of the JAK/STAT signaling ligands Upd3, and Upd2, while maintaining microbiome diversity. These changes likely slow activation of epithelial cell turnover in the gut and contribute to downstream lifespan effects. As the role of INDY and microbiome are conserved across organisms, our study provides a framework to study underlying mechanisms of the effects of reduced Indy and the microbiome on health and longevity.

  PublisherOA PDFDOI

• The interplay between the insect immune system and gut microbiota

  Elsevier eBooks · 2025-08-29

  book-chapterSenior authorCorresponding
  PublisherDOI

• Boosting scientific community values: The impact of social inclusion interventions on biomedical instructors

  Journal of Clinical and Translational Science · 2025-01-01 · 1 citations

  articleOpen access

  Abstract Interventions to foster inclusive learning environments may benefit college STEMM instructors (NASEM, 2019). We investigated the impact of a social inclusion intervention (SII) on scientific self-efficacy, identity, community values, and persistence intentions in a large and diverse sample of biomedical college instructors ( n = 116) in the USA. The results indicated that the SII group developed stronger scientific community values than the control group, and the effect was the strongest for instructors who had initially expressed lower values. From a mentoring perspective, the intervention helps boost feelings of community values, which is linked to increased persistence in STEMM careers.

  PublisherOA PDFDOI

• Tiny Earth CURE Demonstrates Equitable Benefits for U.S. College Science Students

  CBE—Life Sciences Education · 2025-05-29 · 3 citations

  articleOpen access

  Course-based undergraduate research experiences (CURE) enhance student retention in science, technology, engineering, and math (STEM), particularly among students who belong to historically excluded communities. Yet the mechanisms by which CUREs contribute to student integration and persistence are poorly understood. Utilizing the tripartite integration model of social influence (TIMSI), this longitudinal study examines whether and how Tiny Earth-an antibiotic-discovery CURE designed for flexible implementation in a variety of course contexts-impacts students' scientific self-efficacy, scientific identity, endorsement of scientific community values, and intentions to persist in science. The study also explores how gains in TIMSI factors (i.e., scientific self-efficacy, identity, and values) vary as a function of student demographics and course characteristics. A comparison of pre- and postcourse measurements showed that scientific self-efficacy and identity increased among students in Tiny Earth. Some student demographics and course characteristics moderated these gains. Gains in all three TIMSI factors correlated with gains in persistence intentions, whereas student demographics and course characteristics did not. This study shows that the Tiny Earth curriculum equitably improved students' scientific self-efficacy and identity. It also showed that orientation toward scientific values and STEM persistence intentions held steady across most demographic groups.

  PublisherDOI

• Dietary L-3,4-dihydroxyphenylalanine (L-DOPA) augments cuticular melanization in Anopheles mosquitos reducing their lifespan and malaria burden

  Nature Communications · 2025-08-27 · 4 citations

  articleOpen access

  L-3,4-dihydroxyphenylalanine (L-DOPA), a naturally occurring tyrosine derivative, is prevalent in environments that include mosquito habitats, potentially serving as part of their diet. Given its role as a precursor for melanin synthesis we investigate the effect of dietary L-DOPA on mosquito physiology and immunity to Plasmodium falciparum and Cryptococcus neoformans infection. Dietary L-DOPA is incorporated into mosquito melanin via a non-canonical pathway and has a profound transcriptional effect associated with enhanced immunity, increased pigmentation, and reduced lifespan. Increased melanization results in an enhanced capacity to absorb electromagnetic radiation that affects mosquito temperatures. Bacteria in the mosquito microbiome act as sources of dopamine, a substrate for melanization. Our results illustrate how an environmentally abundant amino acid analogue can affect mosquito physiology and suggest its potential usefulness as an environmentally friendly vector control agent to reduce malaria transmission, warranting further research and field studies. Malaria control and elimination require environmentally safe strategies. Here, the authors propose L-DOPA, a naturally occurring tyrosine derivative, as a mosquito dietary intervention that can shorten lifespan and reduce malaria parasite burden of female Anopheles gambiae mosquitoes.

  PublisherOA PDFDOI

• Celebrating the fifth edition of the International Symposium on Fungal Stress – ISFUS, a decade after its 2014 debut

  Fungal Biology · 2025-05-06 · 2 citations

  articleOpen access
  PublisherOA PDFDOI

• Dietary L-3,4-dihydroxyphenylalanine (L-DOPA) augments cuticular melanization in Anopheles mosquitos while reducing their lifespan and malaria parasite burden

  Research Square · 2024-10-16 · 1 citations

  preprintOpen access
  PublisherOA PDFDOI

• Chronic infection alters pathogen virulence, microbiome composition, and fly physiology across generations

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-03-05

  preprintOpen accessSenior authorCorresponding

  Abstract In many insects, parents and offspring share the same environment. Thus, an infection in the parents has the potential to influence offspring defenses. Moreover, infection can also affect other host aspects, including the microbiome, development, and reproduction. To better understand the intergenerational impacts of infection, we assessed the effects of challenge by the gut pathogen Pseudomonas entomophila (Pe) on Drosophila melanogaster . We found that parental challenge by Pe led to environmental transmission of the pathogen from parents to offspring, resulting in a persistent infection among the population. Pe is a highly virulent pathogen; however, we found that persistent infection was correlated with a loss of pathogen virulence across generations. We explored the impact of chronic pathogen exposure on host physiological traits. Our results showed that pathogen load, virulence, and pathogen-induced microbiome remodeling influence fecundity and starvation resistance. Current research in Drosophila and other insects has shown that immune status can be transmitted to the next generation (transgenerational immunity). Since the offspring were continuously exposed to the pathogen, we explored their response to a new infection. Even though we did not find a protective effect, we observed alterations in gene expression and microbiome remodeling following a new Pe challenge that was dependent on the parental treatment. Altogether, our results provide evidence that the pathogen adapted across generations as part of a tolerance mechanism that allows the pathogen to persist in the environment, which confers a greater probability of survival in subsequent generations. However, chronic exposure to the pathogen resulted in a cost to the host by altering several aspects of host physiology. Author summary Infection impacts many aspects of animal physiology, including priming host immune responses to repeated pathogen exposure. Whether parental experiences with a pathogen can influence such responses in offspring is less certain. Here, to further our understanding of generational impacts of infection, we studied the interaction between host immunity, the microbiome, and a gut pathogen across generations using the model organism Drosophila melanogaster. Our results showed that parental challenge established a persistent infection in the population, such that offspring were chronically exposed to the pathogen. This chronic pathogen exposure impacted many host physiological traits, but did not confer protection to re-infection with a high-dose of the pathogen. Instead, we found that the transmitted infection led to a loss of pathogen virulence in offspring. At the same time, pathogen density, virulence, and pathogen-induced microbiome remodeling influenced fecundity and starvation resistance. Overall, our results highlight that infection in parents can influence intergenerational responses due to impacts both on the microbiome and on selection on pathogen virulence. Such chronic interactions with the pathogen, even reduced in virulence, alter host physiology.

  PublisherOA PDFDOI

• Microbiome-derived acidity protects against microbial invasion in Drosophila

  Cell Reports · 2024-04-01 · 28 citations

  articleOpen accessSenior authorCorresponding

  Microbial invasions underlie host-microbe interactions resulting in pathogenesis and probiotic colonization. In this study, we explore the effects of the microbiome on microbial invasion in Drosophila melanogaster. We demonstrate that gut microbes Lactiplantibacillus plantarum and Acetobacter tropicalis improve survival and lead to a reduction in microbial burden during infection. Using a microbial interaction assay, we report that L. plantarum inhibits the growth of invasive bacteria, while A. tropicalis reduces this inhibition. We further show that inhibition by L. plantarum is linked to its ability to acidify its environment via lactic acid production by lactate dehydrogenase, while A. tropicalis diminishes the inhibition by quenching acids. We propose that acid from the microbiome is a gatekeeper to microbial invasions, as only microbes capable of tolerating acidic environments can colonize the host. The methods and findings described herein will add to the growing breadth of tools to study microbe-microbe interactions in broad contexts.

  PublisherOA PDFDOI

• Modulating DNA Polα Enhances Cell Reprogramming Across Species

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-09-20

  preprintOpen access

  Abstract As a fundamental biological process, DNA replication ensures the accurate copying of genetic information. However, the impact of this process on cellular plasticity in multicellular organisms remains elusive. Here, we find that reducing the level or activity of a replication component, DNA Polymerase α (Polα), facilitates cell reprogramming in diverse stem cell systems across species. In Drosophila male and female germline stem cell lineages, reducing Polα levels using heterozygotes significantly enhances fertility of both sexes, promoting reproductivity during aging without compromising their longevity. Consistently, in C. elegans the pola heterozygous hermaphrodites exhibit increased fertility without a reduction in lifespan, suggesting that this phenomenon is conserved. Moreover, in male germline and female intestinal stem cell lineages of Drosophila , polα heterozygotes exhibit increased resistance to tissue damage caused by genetic ablation or pathogen infection, leading to enhanced regeneration and improved survival during post-injury recovery, respectively. Additionally, fine tuning of an inhibitor to modulate Polα activity significantly enhances the efficiency of reprogramming human embryonic fibroblasts into induced pluripotent cells. Together, these findings unveil novel roles of a DNA replication component in regulating cellular reprogramming potential, and thus hold promise for promoting tissue health, facilitating post-injury rehabilitation, and enhancing healthspan.

  PublisherOA PDFDOI

Recent grants

• Non-genetic inheritance: mechanisms of microbiome-mediated transgenerational change

  NIH · $1.9M · 2020–2024

Frequent coauthors

• Jo Handelsman

  University of Wisconsin–Madison

  55 shared

• Gabriel L. Lozano

  Wisconsin Institutes for Discovery

  40 shared

• Danielle Lesperance

  Johns Hopkins University

  27 shared

• Bruno Lemaître

  École Polytechnique Fédérale de Lausanne

  17 shared

• Eric V. Stabb

  University of Illinois Chicago

  14 shared

• Alexander J. Barron

  University of Connecticut

  14 shared

• Amanda Hurley

  Wisconsin Institutes for Discovery

  12 shared

• Luis Balderrama

  Wisconsin Institutes for Discovery

  12 shared

Labs

• Broderick LaboratoryPI

  Focus on characterization of the gut microbiota of insect hosts and study of their impacts on host physiology and susceptibility to disease.

Education

• PhD, Entomology and Microbiology

  University of Wisconsin Madison